Acute intermittent hypercapnic hypoxia augments left ventricular contractility.

IF 4.7 2区 医学 Q1 NEUROSCIENCES
Scott F Thrall, Alex M Williams, Philip J Millar, Megan L Lance, Brooke M Shafer, Conan L H Shing, Jordan D Bird, Christopher R West, Glen E Foster
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引用次数: 0

Abstract

Acute intermittent hypercapnic hypoxia (IHH) evokes persistent increases in vascular sympathetic activity and blood pressure. Whether myocardial contractility is enhanced to contribute to this pressor response is unknown. We hypothesized that IHH would augment left ventricular systolic function. Twenty-four healthy participants (nine females; aged 25 ± 4 years) underwent 40 consecutive 1 min bouts of 40 s of hypercapnic hypoxia ( P ET O 2 ${P_{{\mathrm{ET}}{{\mathrm{O}}_2}}}$ : 48 mmHg; P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_2}}}$ : +5 mmHg) and 20 s of normocapnic normoxia. Cardiac, haemodynamic, respiratory and sympathetic measurements were made at rest and during three 5 min stages of progressive lower body negative pressure (LBNP) (-15, -30 and -45 mmHg) before and after IHH. Following IHH, stroke work [Δ: 64 mJ; 95% confidence interval (CI) = 14-113; P = 0.007], longitudinal strain (Δ: -0.9%; CI = -0.1 to -1.7; P = 0.007) and single-beat estimates of preload-recruitable stroke work (PRSWsb; Δ: 0.9 mJ mL-1; CI = 0.2-1.5; P = 0.004) were enhanced. Across LBNP stages, IHH further enhanced ejection fraction (Δ: 1.0%; CI = 0.0-2.0; P = 0.041), stroke work (Δ: 44 mJ; CI = 23-66; P < 0.001), longitudinal strain (Δ: -0.5%; CI = 0.0 to -0.9; P = 0.047), end-systolic elastance (Δ: 0.15 mmHg mL-1; CI = 0.05-0.25; P = 0.004) and PRSWsb (Δ: 0.60 mJ mL-1; CI = 0.36-0.85; P < 0.001). Linear end-systolic pressure-volume relationships (+0.13 ± 0.06 mmHg mL-1, P = 0.024) and preload-recruitable stroke work slopes (+0.83 ± 0.17 mJ mL-1, P < 0.001) were also increased post-IHH. Ventricular stiffness (E/E' ratio) and relaxation (peak diastolic strain rate) were unaltered by IHH (P > 0.236), whereas the passive/active diastolic filling (E/A) ratio was reduced (P = 0.022), potentially via increased atrial kick contribution (P = 0.068). We demonstrate that increased left ventricular systolic function following acute IHH contributes to the pressor response in addition to the established vasopressor arm in humans. KEY POINTS: Acute intermittent hypercapnic hypoxia evokes persistent sympathoexcitation and increased arterial pressure, known to be mediated by increased vasoconstrictor signalling. Chronic intermittent hypoxia increases cardiac contractility associated with cardiac sympathetic and structural remodelling. However, whether increases in contractility manifest acutely following intermittent hypercapnic hypoxia is unknown. We show increases in indices of cardiac systolic performance at rest and across progressive hypovolaemia following acute intermittent hypercapnic hypoxia. Diastolic relaxation was unchanged, but reductions in the ratio of passive filling to atrial kick during diastole, potentially as a result of increased mitral inflow velocity during atrial filling, suggest that the increases in contractility may extend to the atria.

急性间歇性高碳酸血症性缺氧增强左心室收缩力。
急性间歇性高capic缺氧(IHH)引起血管交感神经活动和血压持续升高。心肌收缩力的增强是否有助于这种升压反应尚不清楚。我们假设IHH会增强左心室收缩功能。24名健康参与者(9名女性;年龄25±4岁,连续40次1分钟40秒高碳酸血症低氧(P ET O 2 ${P_{\ mathm {ET}}{{\ mathm {O}}_2}}}$: 48 mmHg;P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_2}} $: +5 mmHg)和20 s的正碳酸正氧。心脏、血流动力学、呼吸和交感神经测量分别在IHH前后休息时和进行性下体负压(-15、-30和-45 mmHg)的3个5分钟阶段进行。IHH后,冲程功[Δ: 64 mJ;95%置信区间(CI) = 14-113;P = 0.007],纵向应变(Δ: -0.9%;CI = -0.1 ~ -1.7;P = 0.007)和单拍预负荷可恢复卒中功(PRSWsb;Δ: 0.9 mJ mL-1;ci = 0.2-1.5;P = 0.004)。在LBNP分期中,IHH进一步提高了射血分数(Δ: 1.0%;ci = 0.0-2.0;P = 0.041),冲程功(Δ: 44 mJ;ci = 23-66;P 1;ci = 0.05-0.25;P = 0.004)和PRSWsb (Δ: 0.60 mJ mL-1;ci = 0.36-0.85;P -1, P = 0.024)和预负荷可再生卒中工作斜率(+0.83±0.17 mJ mL-1, P 0.236),而被动/主动舒张充盈(E/A)比降低(P = 0.022),可能是通过增加心房踢腿贡献(P = 0.068)。我们证明,急性IHH后左心室收缩功能的增加有助于加压反应,以及人类已建立的血管加压臂。重点:急性间歇性高碳酸血症缺氧引起持续的交感神经兴奋和动脉压升高,已知这是由血管收缩信号增强介导的。慢性间歇性缺氧增加与心脏交感神经和结构重构相关的心脏收缩力。然而,间歇性高碳酸血症低氧是否会导致收缩性增加尚不清楚。我们发现,在急性间歇性高碳酸血症后,静息时和进行性低血容量时心脏收缩性能指标增加。舒张期舒张无变化,但舒张期被动充盈与心房踢跳之比的降低,可能是心房充盈期间二尖瓣流入速度增加的结果,表明收缩性的增加可能延伸至心房。
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来源期刊
Journal of Physiology-London
Journal of Physiology-London 医学-神经科学
CiteScore
9.70
自引率
7.30%
发文量
817
审稿时长
2 months
期刊介绍: The Journal of Physiology publishes full-length original Research Papers and Techniques for Physiology, which are short papers aimed at disseminating new techniques for physiological research. Articles solicited by the Editorial Board include Perspectives, Symposium Reports and Topical Reviews, which highlight areas of special physiological interest. CrossTalk articles are short editorial-style invited articles framing a debate between experts in the field on controversial topics. Letters to the Editor and Journal Club articles are also published. All categories of papers are subjected to peer reivew. The Journal of Physiology welcomes submitted research papers in all areas of physiology. Authors should present original work that illustrates new physiological principles or mechanisms. Papers on work at the molecular level, at the level of the cell membrane, single cells, tissues or organs and on systems physiology are all acceptable. Theoretical papers and papers that use computational models to further our understanding of physiological processes will be considered if based on experimentally derived data and if the hypothesis advanced is directly amenable to experimental testing. While emphasis is on human and mammalian physiology, work on lower vertebrate or invertebrate preparations may be suitable if it furthers the understanding of the functioning of other organisms including mammals.
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